Canine leishmaniasis associated with systemic vasculitis in two dogs

Pumarola, M.; Brevik, L.; Badiola, Juan José; Vargas, Antonia; Domingo, Mariano; Ferrer, L.

doi:10.1016/s0021-9975(08)80196-x

Cited by 57 publications

(49 citation statements)

References 7 publications

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“…PUMAROLA et al (1991) andCIARAMELLA et al (1997) reported vascular lesions in dogs with visceral leishmaniasis triggered by the localized or disseminated deposition of immune complexes in the blood vessel wall. The possibility of deposition of immune complexes in the retina, triggering an inflammatory response and the occurrence of lesions, cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

Histopathological findings and detection of parasites in the eyes of dogs infected naturally with Leishmania chagasi

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Histopathological findings and detection of parasites in the eyes of dogs infected naturally with Leishmania chagasi

et al. 2010

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“…Some authors have suggested the involvement of immune complex deposits in the vascular endothelium or interstitium generating chemotaxis and establishing a local inflammatory response mainly provoking vasculitis in many organs 8,17,22 .…”

Section: Discussionmentioning

confidence: 99%

Chronic interstitial pneumonitis in dogs naturally infected with Leishmania (Leishmania) chagasi: a histopathological and morphometric study

Gonçalves

Tafuri

Melo

et al. 2003

Rev. Inst. Med. trop. S. Paulo

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SUMMARYEighteen mongrel dogs of unknown age and naturally infected with Leishmania (Leishmania) chagasi, were obtained from the City Hall of Belo Horizonte, Brazil. Four dogs were used as control. Lung samples were obtained and immediately fixed in formalin. The histopathological picture of all lung tissue sections was a chronic and diffuse interstitial pneumonitis. The thickened interalveolar septa were characterized by the cellular exudate (mostly macrophages, lymphocytes and plasmocytes) associated with collagen deposition. Morphometric analysis showed greater septal thickness in the infected animals than in controls. In fact, the morphometric study of collagen stained with ammoniac silver confirmed a larger deposition of collagen in the infected animals. The parasitologic method was carried out during the study of the lesions on the slides. However, we did not observe any correlation between the histopathologic and morphometric data and the clinical status of the animals. We conclude that the pulmonary lesions observed in all naturally infected dogs were correlated with the disease and that the morphometric method used was satisfactory for the analysis of septal thickness and of increased collagen deposition, confirming the presence of fibrosis.

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“…17 Occasionally, neurological signs and/or histopathological lesions have been observed affecting the central nervous system (CNS) in CL, 2,9,11 giving rise to the term cerebral leishmaniasis. 8 However, except for the choroid plexuses 13 and meninges, 19 Leishmania amastigotes, to the authors' knowledge, have not been observed in either the CNS parenchyma or peripheral nerves in CL.…”

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“…2 It is thought that a humoral response and deposition of immune complexes are likely responsible for the pathogenesis 2,4 including the systemic necrotizing vasculitis that has been described in affected dogs. 17 Occasionally, neurological signs and/or histopathological lesions have been observed affecting the central nervous system (CNS) in CL, 2,9,11 giving rise to the term cerebral leishmaniasis. 8 However, except for the choroid plexuses 13 and meninges, 19 Leishmania amastigotes, to the authors' knowledge, have not been observed in either the CNS parenchyma or peripheral nerves in CL.…”

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Leishmania amastigotes in the central nervous system of a naturally infected dog

et al. 2012

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Canine leishmaniasis (CL) is a cutaneous, mucocutaneous, or visceral disease caused by intracellular Leishmania protozoan parasites that are transmitted by the bite of female sand flies. Domestic dogs are the main reservoir hosts. The clinical signs are very variable, ranging from subclinical infections to generalized disorders characterized by hyperthermia, anemia, weight loss, polydipsia, hepatomegaly, splenomegaly, hypergammaglobulinemia, generalized lymphadenopathy, cutaneous lesions, and other lesions. 2,4 In visceral CL, parasites and their lesions are found throughout the host organism, producing proliferative inflammatory reactions causing an immune imbalance. Among the inflammatory infiltrates, macrophages predominate, and occasionally amastigotes are found within them. Many organs have been observed to be affected, especially the lymph nodes, liver, spleen, and skin.2 It is thought that a humoral response and deposition of immune complexes are likely responsible for the pathogenesis 2,4 including the systemic necrotizing vasculitis that has been described in affected dogs. 17 Occasionally, neurological signs and/or histopathological lesions have been observed affecting the central nervous system (CNS) in CL, 2,9,11 giving rise to the term cerebral leishmaniasis. 8 However, except for the choroid plexuses 13 and meninges, 19 Leishmania amastigotes, to the authors' knowledge, have not been observed in either the CNS parenchyma or peripheral nerves in CL. The current study described a dog with radiculoneuritis, myelitis, and mild meningoencephalitis associated with Leishmania spp. amastigotes in the peripheral and central nervous systems.A 4-year-old male Labrador Retriever suffered an episode of left hemiparesis 9 months before presentation. Blood analysis at that time showed thrombocytopenia and mild hyperglobulinemia. Enzyme-linked immunosorbent assay (ELISA) a for anti-Leishmania antibodies and indirect fluorescent antibody test (IFAT) b for Leishmania were negative. The animal responded favorably to chronic treatment with prednisolone.c Seven months later the animal relapsed, and blood analysis revealed anemia, hyperproteinemia, hypoalbuminemia, and hyperglobulinemia. A second ELISA a test was performed and the result was again negative. Serology for Toxoplasma and Neospora was negative. At that time, treatment was begun with clindamycin, d and an improvement in the clinical signs was noted.Forty-five days later, the dog was referred to the Al Sur Veterinary Hospital with a 10-day evolution of tetraplegia. Clinical examination showed hypothermia, dehydration, tachypnea, and cachexia. The animal was depressed, and postural reactions were absent. Carporadialis and flexor reflexes in the forelimbs were absent; bilateral Horner syndrome was also observed. Atrophy of the supra and left spinal nerves. Microscopically, nerve fiber destruction together with mixed inflammatory infiltration was observed in the spinal nerves. Cervical spinal cord sections showed multifocal, diffuse granulomatous inflammation ...

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Canine leishmaniasis associated with systemic vasculitis in two dogs

Cited by 57 publications

References 7 publications

Histopathological findings and detection of parasites in the eyes of dogs infected naturally with Leishmania chagasi

Histopathological findings and detection of parasites in the eyes of dogs infected naturally with Leishmania chagasi

Chronic interstitial pneumonitis in dogs naturally infected with Leishmania (Leishmania) chagasi: a histopathological and morphometric study

Leishmania amastigotes in the central nervous system of a naturally infected dog

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